In 2009 a novel swine-origin H1N1 virus emerged in humans, resulting in the first influenza pandemic of the 21st century. This A(H1N1)pdm09 (pH1N1) virus has continued to circulate and was the predominant strain in the USA during the most recent 2013/14 influenza season (CDC. Update: influenza activity-United States, Sep. 29, 2013-Feb. 8, 2014. MMWR 63, 148-54 (2014)). Although the overall disease incidence was lower in the 2013/14 winter than during the 2009 outbreak, adults 18-64 years old were at higher risk of severe disease and death when compared to the traditionally highest risk 65+ year age group. This corresponded to a low rate of vaccination in young adults (CDC. FluVaxView. Centers for Disease Control and Prevention, available on the internet <cdc.gov/flu/fluvaxview/1314season_htm>. (2014)). Fortunately, most pH1N1 viruses are sensitive to the clinically available NA inhibitors oseltamivir and zanamivir, and therefore patients can be offered treatments early after infection (Moscona, A. N Engl J Med 353, 1363-73 (2005)). Oseltamivir is often the treatment of choice because it is available as an oral formulation and therefore easier to administer than inhalation of zanamivir. However, NA inhibitor-resistant influenza viruses can be selected quickly in treated patients (Memoli, M. J. et al. J Infect Dis 203, 348-57 (2011)), or can sometimes emerge without an apparent link to treatment (Sheu, T. G. et al. Antimicrob Agents Chemother 52, 3284-92 (2008)). Indeed, during the 2013/14 influenza season, oseltamivir-resistant pH1N1 viruses were reported in China, Japan and the USA (WHO. World Health Organization, see the internet at <.who.int/influenza/vaccines/virus/recommendations/2014_15_north/en/> (2014)). The increased pH1N1 influenza activity and the emergence of oseltamivir-resistant pH1N1 viruses add urgency to the need for additional influenza antivirals. It would be advantageous for the new therapeutics to inhibit influenza virus through mechanisms distinct from oseltamivir and zanamivir, to help assure that NA inhibitor-resistant viruses remain sensitive to the new agents.